EFFECT OF DIET ON ENERGY METABOLISM
饮食对能量代谢的影响
基本信息
- 批准号:3483132
- 负责人:
- 金额:$ 13.78万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:1976
- 资助国家:美国
- 起止时间:1976-05-01 至 1995-07-31
- 项目状态:已结题
- 来源:
- 关键词:adrenal glands adrenalectomy animal age group basal metabolism bioenergetics biological models body temperature brain metabolism brown fat corticosterone diet dietary constituent experimental brain lesion fasting genetic strain hormone regulation /control mechanism hypothalamus insulin laboratory mouse laboratory rat liver metabolism neuroendocrine system neurotransmitter metabolism norepinephrine nutrition related tag obesity pancreatic islets pathogenic diet protein metabolism sympathetic nervous system thyroid hormones
项目摘要
Obese (ob/ob) mice and rats with obesity-producing hypothalamic
knife-cuts become obese even if pairfed to their respective
controls. These animals must therefore expend less energy than
normal. Our overall goal is to identify neuroendocrine and
cellular factors responsible for the enhanced efficiency of dietary
energy retention in these obese animals. Experiments are
proposed to determine why adrenalectomy blocks further
development of obesity in ob/ob mice fed a high-starch diet, but
not in ob/ob mice fed high-glucose or high-fat diets. Effects of
these dietary treatments on neural control of insulin secretion by
isolated pancreatic islets, on unidirectional uptake of thyroid
hormones and corticosterone by liver and brain, on sympathetic
nervous system activity in heart and brown adipose tissue as
assessed by norepinephrine turnover, on brown adipose tissue
thermogenic capacity, and on the involvement of
thermoregulatory thermogenesis in energy balance in sham-
operated and adrenalectomized ob/ob and lean mice will be
ascertained. The hypotheses that the central nervous system is
the site of glucorticoid action responsible for development of
obesity in ob/ob mice, and that hyperinsulinemia is the critical
mediator of glucorticoid-induced obesity in ob/ob mice will be
evaluated. Selective comparisons between ob/ob mice and rats
with hypothalamic knife-cuts will help identify the key factors
that permit high retention of dietary energy in these animals.
These data should increase our understanding of the diet-
dependent metabolic factors in development of obesity, and
should aid in defining improved nutritional approaches to cope
with the prevention and control of obesity.
具有产生肥胖的下丘脑的肥胖 (ob/ob) 小鼠和大鼠
即使与各自的人配对,刀切也会变得肥胖
控制。 因此,这些动物消耗的能量必须比
普通的。 我们的总体目标是确定神经内分泌和
负责提高饮食效率的细胞因素
这些肥胖动物的能量保留。 实验是
提议确定肾上腺切除术进一步阻止的原因
喂食高淀粉饮食的 ob/ob 小鼠会出现肥胖,但是
在喂食高葡萄糖或高脂肪饮食的 ob/ob 小鼠中则不然。 的影响
这些饮食疗法对胰岛素分泌的神经控制
孤立的胰岛,单向摄取甲状腺
肝脏和大脑通过交感神经产生激素和皮质酮
心脏和棕色脂肪组织中的神经系统活动
通过棕色脂肪组织上的去甲肾上腺素周转率进行评估
产热能力,以及参与
假手术中能量平衡中的温度调节产热作用
手术和肾上腺切除的 ob/ob 和瘦小鼠将
确定。 中枢神经系统的假设
糖皮质激素作用位点负责发展
ob/ob 小鼠肥胖,高胰岛素血症是关键
糖皮质激素诱导的 ob/ob 小鼠肥胖的介质是
评价。 ob/ob 小鼠和大鼠之间的选择性比较
下丘脑刀切将有助于确定关键因素
允许这些动物高度保留膳食能量。
这些数据应该会增加我们对饮食的理解——
肥胖发展中的依赖代谢因素,以及
应有助于确定改进的营养方法来应对
与预防和控制肥胖有关。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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